Propofol facilitated excitatory postsynaptic currents frequency on nucleus tractus solitarii (NTS) neurons

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• 作者：Zhenhua Jin^a ; Myung-Jin Choi^a ; Cheung-Seog Park^b ; Young Seek Park^b ; Young-Ho Jin^a ; ^{jinyh@khu.ac.kr}
• 关键词：NTS ; Nucleus tractus solitarii ; sEPSCs ; Spontaneously occurring EPSC events ; [Cl&minus ; ]i ; Intracellular Cl&minus ; concentration ; ECl&minus ; Equilibrium potential for Cl&minus ; EGABA ; Reversal potential for GABAA receptor-mediated currents ; NKCC1 ; Na+-K
• 刊名：Brain Research
• 出版年：2012
• 出版时间：13 January 2012
• 年：2012
• 卷：1432
• 期：Complete
• 页码：1-6
• 全文大小：515 K

文摘

Propofol, an intravenous anesthetic, is broadly used for general anesthesia and diagnostic sedations due to its fast onset and recovery. Propofol depresses respiratory and cardiovascular reflex responses, however, their underlying mechanisms are not well known. Cardiorespiratory information from visceral afferent vagus nerves is integrated in the nucleus tractus solitarii (NTS). Cardiac and respiratory signals transducing vagal afferent neurons release the excitatory neurotransmitter glutamate onto NTS neurons in an activity dependent manner and trigger negative feedback reflex responses. In this experiment, the effects of propofol on glutamatergic synaptic responses at NTS neurons was tested using patch clamp methods. Glutamatergic excitatory postsynaptic currents (EPSC) were recorded at chloride reversal potential (?#xA0;49 mV) without ¦Ã-aminobutyric acid type A (GABA_A) receptor antagonists. Propofol (?#xA0;3 ¦ÌM) facilitated frequency of the spontaneous EPSCs in a concentration dependent manner without altering amplitude and decay time. The GABA_A receptor selective antagonist, gabazine (6 ¦ÌM), attenuated propofol effects on glutamate release. Propofol (10 ¦ÌM) evoked glutamate release was also blocked in the presence of the voltage dependent Na⁺ and Ca²⁺ channel blockers TTX (0.3 ¦ÌM) and Cd²⁺ (0.2 mM), respectively. In addition, the Na⁺-K⁺-Cl^{?/sup> cotransporter type 1 antagonist bumetanide (10 ¦ÌM) also inhibited propofol evoked increase in sEPSC frequency. These results suggest that propofol evoked glutamate release onto NTS neurons by GABA_A receptor-mediated depolarization of the presynaptic excitatory terminals.}